Liquid crystal monomers induce placental development and progesterone release dysregulation through transplacental transportation

Embryonic and fetal development can be affected during gestation by exposure to xenobiotics that cross the placenta. Liquid crystal monomers (LCMs) are emerging contaminants commonly found in indoor environments; however, whether they can cross the placenta and affect placental development remains unexplored. Here, we developed an evaluation system that integrates human biomonitoring, uterine perfusion in pregnant rats, and placental cells. We found fourteen out of the fifty-six LCMs that were detected in maternal and cord serum samples from ninety-three healthy pregnant women, at median levels of 13.9 and 18.1 ng/mL, respectively. Subsequent exploration of in utero exposure in rats indicated that aromatic amino acid transporter 1 (SLC16A10) mediated transplacental transportation of the LCMs. Placental cells exposed to LCMs exhibited delayed placental development and reduced progesterone release. These findings showed that SLC16A10-mediated transplacental transportation of LCMs inhibits placental development and progesterone release, highlighting the importance of gestational exposure to emerging contaminants.

妊娠期间，穿过胎盘屏障的外源性化学物（xenobiotics）可对胚胎与胎儿发育造成影响。液晶单体（Liquid Crystal Monomers，LCMs）是一类常见于室内环境的新兴污染物，但其能否穿过胎盘屏障并影响胎盘发育仍未被探明。本研究构建了一套整合人体生物监测、妊娠大鼠子宫灌注实验及胎盘细胞实验的评估体系。我们在93名健康妊娠女性的母体血清与脐带血清样本中，检出了56种液晶单体中的14种，二者的中位浓度分别为13.9 ng/mL与18.1 ng/mL。后续针对大鼠子宫内暴露的研究显示，芳香族氨基酸转运蛋白1（SLC16A10）介导了液晶单体的胎盘跨膜转运。暴露于液晶单体的胎盘细胞表现出胎盘发育迟缓以及孕酮释放量降低的现象。上述研究结果证实，SLC16A10介导的液晶单体胎盘跨膜转运可抑制胎盘发育与孕酮释放，凸显了妊娠期间暴露于新兴污染物的重要性。